Functional and gene expression profiles to provide clues to the mechanisms involved in susceptibility or resistance of skeletal muscle cells to ZIKV infection

The Zika virus (ZIKV) is an arthropod-borne virus (arbovirus) and belongs to the Flaviviridae family. The main manifestation of the Congenital Zika syndrome is the severe malformation of the central nervous system as well as congenital contractures such as arthrogryposis. Neuromuscular comorbidities are highly prevalent in children that have been congenitally infected by the ZIKV. Microcephaly and arthrogryposis occur during the fetal phase and infancy, when myoblasts are continually merging into myotubes to promote muscle growth. It has been demonstrated that human primary myoblasts can be infected by ZIKV in vitro, whereas myotubes are rather resistant to infection, suggesting that muscle cells can account for a peripheral site of viral amplification, which in turn, may contribute to the pathophysiology of Zika infection. In this study we aim to analyze functional and gene expression profiles to provide clues to the mechanisms involved in susceptibility or resistance of skeletal muscle cells to ZIKV infection.